Simmaron’s next immune study: where’s the weak link?

Simmaron Research has a new immune study, building on all the exciting research that is changing how we think about ME/CFS.

Twenty years ago the internationally known virus hunter, Dr. Ian Lipkin of Columbia University, didn’t find Borna Virus in people with ME/CFS, but he never forgot the immune dysfunction he found. Twenty years later he found more immune dysfunction in another study.

He doesn’t know why it’s there but he does believe that all ME/CFS cases – no matter what pathogen or other factor has triggered them – devolve to a ‘common pathway’. The fact that pathogens of all types – from Epstein-Barr Virus, to SARS, to Giardia – can trigger ME/CFS indeed suggests a core immune deficiency lies at the heart of the illness.

Every genetic study suggests an inherited susceptibility to Chronic Fatigue Syndrome is present. Dr. Mady Hornig of the Center for Infection and Immunity at Columbia University believes that a genetic predisposition in combination with an environmental trigger (such as an infection) occurring at just the right (wrong) time is probably key to coming down with ME/CFS.

For thirty or forty years you might be able to easily slough off this bug or that pathogen, but at some point for some reason the stars aligned; you were depleted in just the right way, the pathogen hit and with your immune system genetically predisposed to crack under the pressure – it did – and your entire system faltered.

Simmaron Research’s next pilot study is looking for that immune crack in the dike – the genetic underpinnings of the system collapse that occurred. Led by Simmaron’s Scientific Director, Isabel Barao, PhD, in collaboration with researchers at the National Cancer Institute and University of Nevada Reno, it will determine if your NK and B-cells and macrophages are genetically predisposed to respond poorly to a virus, toxin, or cancer cell.

Dr. Barao is studying whether people with ME/CFS have polymorphisms – unusual gene formations – that make their key immune cells less likely to respond well to viruses and other threats. That immune ‘hole’ many people have talked about with regards to ME/CFS could start here. We all know about the rampant NK cell problems in ME/CFS, but this study could help explain the B-cell problems recently uncovered in a German research study – and perhaps even shed light on why Rituximab may be working in some patients.

It’s the initial part of a projected three-part study that could end with drugs for ME/CFS. Once genetic alterations have been found, they’ll be correlated with immune findings. If that holds up, it’s time to look for drugs to fix the problem, two of which are currently in clinical trials.

Think about it. The high heritability rates in ME/CFS indicate genetic problems exist somewhere. Where better to look than the immune system?

This is a no-brainer to me. It’s relatively cheap – it has a quick six-month turnaround – and the data it produces will lay the foundation for an NIH grant on topics well recognized as important by immunologists (NK and B cells).